Treatment of Glaucoma

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The term Glaucoma includes a number of optic neuropathies that share certain commonalities. Together they make up the leading cause of irreversible blindness worldwide, estimated to affect 80 million people by 2020. In the first, these neuropathies are characterized by a progressive vision loss due to dysfunction and degeneration of retinal ganglion cells in the eye. Glaucoma may have a genetic component where family history and ethnicity increase its likelihood. Glaucoma is divided into two main types including open-angle and closed-angle glaucoma. Although the dysfunction and degeneration of retinal ganglion cells and their projections are what cause blindness in glaucoma, existing therapies target lower intraocular pressure(IOP) through medication or surgery. The primary line treatment for glaucoma is the topical use of eye drops to reduce intraocular pressure.  There are five classes of intraocular pressure-lowering drugs, all of which either reduce the production of aqueous humor(AH) by reducing the activity of the ciliary body or increase AH outflow by action on the drainage canals in the iridocorneal angle. The lowering  IOP often slows the progression of vision loss even in patients with normal intraocular pressure.

     Aqueous humor(AH) can be reduced with drugs targeting the adrenergic system, antagonizing β-and activating the α-receptor such as (Timolol or Brimonidine) or with carbonic anhydrase inhibitors such as (Dorzolamide), presumably by slowing the formation of bicarbonate ions with a subsequent reduction in Na ion and fluid transport. Aqueous humor outflow can be increased by a prostaglandin analog (e.g, Latanoprost, a prostaglandin F analogs) or agonists of adrenergic and cholinergic signaling(e.g, carbachol).

   A patient who is unresponsive to these medications or has other issues can undergo surgery to physically increase aqueous humor(AH) outflow by creating new drainage canals in the eye. Shunts or cannulae used as drainage devices may also be implanted.

 

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